Linked Life Data

11801450

Source:http://linkedlifedata.com/resource/pubmed/id/11801450

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2002-1-21
pubmed:abstractText
The crucial clinical problem in leprosy is the occurrence of acute inflammatory episodes that lead to nerve damage, even after the infecting organisms have been killed by antibiotics. We suggest that the instability of these inflammatory sites is attributable to a disturbance of the role that nerves play in the regulation of inflammation. The destruction of sensory C fibers and sympathetic innervation will remove anti-inflammatory feedback circuits. Moreover, diminishing levels of neuropeptides and changes in the cytokine profile will affect the cortisol-sensitivity of infiltrating T cells, and modulate the cortisol-cortisone shuttle so that the inflammatory site becomes resistant to physiological levels of anti-inflammatory adrenocortical steroids.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1471-4906
pubmed:author
pubmed:issnType
Print
pubmed:volume
23
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
18-22
pubmed:dateRevised
2005-11-16
pubmed:meshHeading
pubmed:year
2002
pubmed:articleTitle
Can nerve damage disrupt neuroendocrine immune homeostasis? Leprosy as a case in point.
pubmed:affiliation
Dept Medical Microbiology, Windeyer Institute of Medical Sciences, Royal Free and University College Medical School, 46 Cleveland Street, W1P 6DB, London, UK. g.rook@ucl.ac.uk
pubmed:publicationType
Journal Article, Review